Meeting Abstract

17-5   11:00 - 11:15  Genetic variance in phenotypic responsiveness of Anolis lizards to testosterone Wittman, TN; Robinson, CD; Cox, RM*; University of Virgina rmc3u@virginia.edu

Hormones structure phenotypic integration by simultaneously regulating the expression of multiple traits. This hormonal pleiotropy is thought to emerge from the regulatory effects of hormones of hundreds to thousands of underlying genes, which collectively harbor genetic variance in hormonally regulated phenotypes. Because hormones link genes to phenotypes in this way, we hypothesized that (1) hormonal pleiotropy should structure patterns of genetic variance and covariance for hormonally regulated phenotypes, and (2) these same phenotypes should also exhibit genetic variance in their responsiveness to hormonal signals. To test these hypotheses, we combined a paternal half-sib breeding design in a large, captive-bred population of brown anole lizards (Anolis sagrei) with an experiment in which we treated half of the progeny in each full-sib family with a testosterone implant at three months of age, while giving their siblings an empty implant as a control. Phenotypically, testosterone masculinized females by increasing body size and altering the area, hue, saturation, and brightness of the dewlap, a sexually dimorphic ornament. In support of our first hypothesis, we found that treatment of females with testosterone eliminated natural sex differences in additive genetic variances and covariances for these phenotypes and increased the strength of genetic correlations between the sexes. In support of our second hypothesis, we found that some phenotypes (dewlap hue and brightness) exhibited significant additive genetic variance in their responsiveness to testosterone, whereas others (dewlap area and saturation) did not, despite underlying genetic variance in each phenotype. Our results support the view that hormonal pleiotropy structures genetic covariance in phenotypes, and that hormonal pleiotropy itself is underlain by genetic variance in the responsiveness of phenotypes to hormonal signals.